Review

Tremor: Clinical Phenomenology and Assessment Techniques

Christopher W. Hess1

& Seth L. Pullman1*

1 Clinical Motor Physiology Laboratory, Department of Neurology, Columbia University Medical Center, New York, New York, United States of America

Abstract

Background: Tremors are among the most common movement disorders. As there can be considerable variability in the manner in which clinicians assess

tremor, objective quantitative tools such as electromyography, accelerometry, and computerized, spiral analysis can be very useful in establishing a clinical diagnosis

and in research settings.

Methods: In this review, we discuss the various methods of quantitative tremor analysis and the classification and pathogenesis of tremor. The most common

pathologic tremors and an approach to the diagnosis of tremor etiology are described.

Conclusions: Pathologic tremors are common, and the diagnosis of underlying etiology is not always straightforward. Computerized quantitative tremor analysis

is a valuable adjunct to careful clinical evaluation in distinguishing tremulous diseases from physiologic tremors, and can also help shed light on their pathogenesis.

Keywords: Tremor, Parkinson disease, essential tremor, dystonia, orthostatic tremor, motor physiology

Citation: Hess CW, Pullman SL. Tremor: clinical phenomenology and assessment techniques. Tremor Other Hyperkinet Mov 2012;2: http://tremorjournal.org/

article/view/65

* To whom correspondence should be addressed. E-mail: sp31@columbia.edu

Editor: Elan D. Louis, Columbia University, United States of America

Received: September 18, 2011 Accepted: November 23, 2011 Published: June 28, 2012

Copyright: ’ 2012 Hess et al. This is an open-access article distributed under the terms of the Creative Commons Attribution–Noncommercial–No Derivatives License, which permits

the user to copy, distribute, and transmit the work provided that the original author(s) and source are credited; that no commercial use is made of the work; and that the work is not altered

or transformed.

Funding: This work was supported, in part, by the Parkinson’s Disease Foundation. S.L.P is partially supported by NIH grant # NS042859, the Parkinson Disease Foundation, and the

Michael J. Fox Foundation.

Financial Disclosures: None.

Conflict of Interest: S.L.P serves on the scientific advisory board of Musicians with Dystonia, Dystonia Medical Research Foundation, on the editorial board of Neurological Bulletin,

and this journal, Tremor and Other Hyperkinetic Movements. He has a United States Patent 6,454,706 (2002) ‘‘System and Method for Clinically Assessing Motor Function.’’ C.W.H has

nothing to disclose.

Introduction

Tremor is among the most common movement disorders and is

characterized by rhythmic oscillations of a part of the body around one

or more joints.1 Methods of tremor assessment include simple clinical

observation, standardized rating scales, objective clinical assessment of

drawn figures, and computerized tremor analysis. A broad overview of

tremor, and the relative advantages and disadvantages of tremor

assessment methods are discussed below. As there are different kinds of

tremor with numerous underlying causes, the process of tremor

classification and evaluation is of critical importance to establish a

correct diagnosis and initiate the most appropriate treatment.

Classification of tremor

Tremor can be most effectively classified based on the circumstances

under which it occurs.

Rest tremor can be distinguished from other forms of tremor based

on its occurrence when the tremoring body part is completely

supported against gravity without voluntary muscle contraction, in

contrast to action tremor, which occurs with voluntary muscle

contraction.2 Action tremor can be further divided into postural or

sustention tremor (occurring while maintaining a posture against

gravity) and kinetic tremor (occurring during active movement).

Kinetic tremor includes task-specific tremor and tremor that is specific

to goal-directed movements (intention tremor). It can also be associated

with situations where there is active muscle contraction against a

fixed object (isometric tremor). While the tremors encountered in

clinical practice are usually involuntary, patients can present with

psychogenic tremor in isolation or in combination with other neurologic

complaints of psychogenic origin, as in psychogenic parkinsonism.2

In addition to provoking circumstances, other tremor characteristics

Freely available online

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have been used to try to classify tremor (such as frequency,

amplitude, or distribution). However, such classifications are often

problematic as these characteristics can vary greatly within tremor

etiologies.

Evaluation of tremor

Though tremor may be the most quantifiable of all movement

disorders, there is currently no universally accepted method of rating

or measuring tremor.3,4 There can be considerable variability in the

manner in which clinicians assess the presence of tremor and its

severity. In an attempt to standardize the evaluation of tremor

(particularly for clinical research purposes), a number of rating scales

have been developed that optimize comparability between studies and

patient populations.5 One of the earlier tremor scales developed that is

still in use today is the Fahn–Tolosa–Marin Tremor Rating Scale

(TRS).6 This 5-point scale rates tremor severity based on tremor

amplitude, from 0 (no tremor) to 4 (severe tremor) in each part of the

body, and includes assessments of specific abilities and functional

disability. A number of other scales have been developed, which

include smaller severity gradations7 or are disease specific.5,8 Although

tremor scales vary regarding reliability and validity,5,9,10 even the best

clinical scale may not be sensitive enough to discern minimal

abnormality and subtle changes over time, or objective enough to

determine significant responses to therapy. While graphic evidence of

tremor activity can be evaluated clinically by examining writing or

drawn spirals, these are still interpreted subjectively and are not easily

standardized across subjects. Thus, the objective and quantifiable data

analysis afforded by computerized assessment of tremor can be an

important tool in research and certain clinical settings.11

Computerized tremor analysis

Because tremors are quasi-sinusoidal movements, they are amenable

to quantitative mathematical analysis and modeling with a high degree

of fidelity to the clinical picture. To record tremor activity,

accelerometry, electromyography (EMG), and other signals (such as

force or gyroscopic measurements) are acquired, digitized through an

analog-to-digital board and analyzed. With modern computers and

digital signal processing boards, tremors can be analyzed in real time at

a high sampling rate or processed off-line. Additional assessments (such

as time series analyses) can detect complex synchronization and signal

relationships within tremors.

Two of the most important characteristics of tremor assessed by

tremor analysis are frequency and amplitude. Tremor frequency, or

the amount of oscillations per second, is measured in cycles per second

(Hz). If the number of sampled points is N over a period of time T in

seconds, then the sampling rate is N/T, the frequency resolution is

1/T Hz and the maximum recordable frequency is N/2T Hz (also

known as the Nyquist frequency).12 Thus, if the highest frequency of

concern is 25 Hz (most biological tremors fall in lower frequency

ranges), the sampling rate of the recording device must be at least

50 Hz (and preferably several times that) for better signal processing.

Low-pass filtering and other techniques can be used to further improve

signal-to-noise ratios. Depending on recording circumstances, tremor

frequencies can be reliably calculated to within 0.1 Hz and tremor

displacement amplitudes can be determined accurately to less than

0.1 mm. It is important to remember, however, that frequency

determination alone is not sufficient for a diagnosis as there is

considerable frequency overlap between conditions.

While tremors are typically described by their frequency (such as

parkinsonian rest tremor ranging from 3 to 6 Hz), patients are usually

not greatly bothered by tremor frequency, but rather by the amplitude

of their tremor.13,14 Therefore, with regard to clinical disability and

therapeutic effect, amplitude and other waveform characteristics may

be more important.15 The degree of linear or angular displacement of

the limb or body part, or the tremor amplitude, is generally measured

in millimeters or degrees. Tremor amplitude can be accurately

assessed using accelerometers or gyroscopes. Miniature accelerometers

can be attached to the involved tremulous parts of the body, typically

the limbs and occasionally the head, neck, or trunk, and do not

interfere with voluntary or involuntary movements. High-powered

microcomputers, now capable of recording and analyzing large

amounts of data quickly and efficiently, give almost instantaneous

displacement from accelerometric signals. Furthermore, such opera-

tions can be modified to also filter out low-frequency noise such as

unwanted drift or higher frequency electronic interference.

Accelerometric or gyroscopic data can be difficult to appreciate

clinically because sinusoidal motion is not easily perceived in

accelerometric or rotational units; however, with mathematical

integration, displacement of the oscillating body part can be derived

from these signals.

EMG provides additional useful information about the activity of

muscles involved in the generation of tremor. EMG activity may be

recorded using needle, wire electrodes, or more typically surface

electrodes overlying active muscles.16 The EMG can provide

information about motor unit recruitment and synchronization,4,17

and can also elucidate the relationship between involved muscles and

tremulous movements, revealing whether antagonist muscles (such as

flexors and extensors of the wrist) are working at the same time or

alternately to produce tremor. To utilize the EMG most appropriately

in tremor analysis, the signal has to be processed by rectification and

integration or smoothing to place its frequency profile into the tremor

range.4

The objective and detailed findings of a tremor analysis test are most

helpful when the clinical picture is complicated or when clinical signs

are subtle.18 For example, parkinsonian tremor and essential tremor

(ET) can sometimes be difficult to separate clinically, but diagnosis is

obviously important to distinguish the appropriate prognosis and

treatment.1,13,19,20 Both conditions occur with increasing age, and

both may occur at rest, with postures, or during voluntary movements.

EMG-to-movement, side-to-side frequency relationship, EMG topo-

graphy, reflex responses, tremor amplitude ratios during different

clinical tasks, and methods such as time series analyses are ways by

which quantified analysis can be diagnostically useful.

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Computerized tremor analysis can also shed light on the manner in

which tremor is perceived and graded by clinician observers.21 In

evaluating and grading change in tremor severity, the change in

tremor amplitude perceived by a clinician is governed by Weber–

Fechner laws of psychophysics, in which the size of the discernible

change is proportional to the initial tremor amplitude, with a

logarithmic relationship between tremor amplitude and perceived

change in amplitude, despite the apparent linearity of clinical

scales.21–23 A combined study of tremor analysis data from five

different laboratories confirmed this non-linear relationship and

demonstrated good correlation between computerized tremor analysis

and 4- and 5-point tremor rating scales in this context.21

In addition to tremor analysis using accelerometry and EMG,

tremor can also be evaluated through the quantification of drawn

spirals (Figure 1).

Archimedean spirals drawn on a digitizing tablet can be analyzed in

both the x–y plane of the tablet and the z plane of pen pressure

perpendicular to the tablet. By mathematically ‘‘unraveling’’ drawn

spirals and averaging multiple trials together, tremor characteristics

such as frequency, direction, and amplitude can be detected and

quantified, as well as an abundance of other variables, including

drawing speed and acceleration, loop-to-loop width tightness and

variation, and drawing pressure over time.11 Owing to its portability

and ease of data acquisition, which can be analyzed offline, spiral

analysis lends itself particularly well to the demonstration and

quantification of subtle motor abnormalities in patient cohorts that

might not be appreciated using standard clinical rating scales.24

Tremor pathogenesis

Physiologic tremor (PT), like all tremors, is generated and mediated

both peripherally and centrally. The peripheral component of PT

contributes irregular very low amplitudes and variable (8–12 Hz and

higher) oscillations depending on the mass, stiffness, and other

properties of the tremoring body part. It is a passive response caused

by disturbances such as cardioballistics, mild physical perturbations,

and subtetanic motor unit firing (too few motor units discharge

together to result in anything but imperceptible movement or force).3,4

In addition to mechanical factors, short and long loop reflexes

influence the peripheral component, although to a lesser degree.

Hence, the peripheral component is often termed ‘‘mechanical reflex.’’

If the peripheral component can be detected (which is not always the

case), inertial loading (weighting) and other mechanical alterations

affect it simply by changing limb physical properties.25 Inertial loading

will decrease the mechanical-reflex frequency component in the same

manner as weighting slows down a clock pendulum. However, because

of non-linearities in the nervous system (spindle stretch responses,

muscle properties changes with length, thixotropy, neural membrane

firing characteristics, etc.), inertial loading effects are not simple and

must be interpreted cautiously. Furthermore, the mechanical-reflex

component is not always detectable.

The central component of PT, often referred to as the ‘‘central

oscillator’’, contributes weak 8–12 Hz very low-amplitude movements.

The central oscillator of PT is not greatly affected by inertial loading or

other physical manipulations. Motor units are not entrained (dischar-

ging in groups) in PT. When they become entrained, e.g., due to stress,

drugs, or cold (as in shivering), PT develops into exaggerated

physiologic tremor (EPT). EPT has the same peripheral and central

components as PT, but there is greater participation of the stretch

reflex and of the 8–12 Hz central oscillator. When EPT becomes

clinically symptomatic with posture or movement without provoking

factors, it becomes phenomenologically similar to ET and may be

difficult to separate from EPT early in its course.

Pathologic tremors such as ET, dystonic tremor (DT), or the tremors

of Parkinson disease (PD) result in a variety of tremor frequencies from

about 1–25 Hz. They are thought to be generated centrally and

usually obfuscate their peripheral components (except in neuropathic

tremor). The etiology of tremor in PD is poorly understood, but based

on recent magnetoencephalography and imaging studies is thought to

involve networks of both cortical and subcortical areas.26,27 While

traditionally considered a functional monosymptomatic condition, an

accumulation of both epidemiologic and pathologic studies have

argued that ET may be a neurodegenerative disease with both an

increased risk of non-tremulous co-morbidities28 and structural

pathologic changes in the cerebellum.29 It is generally believed that

the tremors in ET have contributions secondary to abnormal

oscillatory activity either within the cerebellum30 or in the olivocer-

ebellothalamic pathway.31

Approach to the diagnosis of tremor

The most practical approach to understanding tremors is to classify

them phenomenologically according to the circumstances under which

they occur, in conjunction with the clinical history and exam, as well as

by appropriate testing when warranted (Table 1).

Rest tremors

Rest tremors most often occur in the setting of PD or parkinsonism.

PD rest tremors typically start unilaterally and distally as the classic 3–

6 Hz ‘‘pill-rolling’’ sinusoidal oscillations, and progress more

proximally as they generalize to both sides, though tremor may

occasionally start anywhere (such as in the jaw). Early in the disease,

tremor amplitude fluctuates significantly with mental or physical

demands and thus is often described as intermittent. Oscillations in

wrist extension and flexion, pronation and supination, or finger flexion

(producing the pill-rolling quality) can be seen.4 As with most

movement disorders, PD tremor is worsened by stress (which can be

useful to bring out tremor during clinical evaluation) and disappears

during sleep. Anxiolytics or alcohol can improve symptoms simply by

reducing anxiety, which may lead to confusion as ET is specifically

responsive to alcohol.

A poly-EMG profile of PD rest tremor typically shows alternating

(less commonly synchronous) contraction of agonist and antagonist

muscles at a frequency of less than 6 Hz with relatively sinusoidal

displacement on accelerometric tracings (Figure 2).

Tremor Phenomenology and Assessment Hess CW, Pullman SL

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Figure 1. Representative Quantitative Spiral Analyses for Normal Subjects, Parkinson Disease (PD), and Essential Tremor (ET) PatientsDemonstrating Tremor Frequency Spectra and Axis. Row 1: Original spiral drawings in 10 6 10 cm outlines with two line colors denoting the left and right

sides of the spiral. Row 2: The spirals with dimension of time (seconds) in the vertical axis demonstrating temporal executions of the spirals. Row 3: The graphic

representations of spiral unraveling where the x-axis 5 angle (radians) and the y-axis 5 radius (cm). Row 4: Spectral analyses of spiral tremor frequencies where the

x-axis 5 frequency (Hz) and y-axis 5 frequency power. Row 5: Tremor axes, when present, illustrating the predominant direction of spiral tremors.

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In tremor that is bilateral, tremor frequencies are similar. Some

studies have found high coherence between limbs (despite amplitude

asymmetry) for brief periods of time,32 though this is not always

observed.33,34

While tremor severity does not correlate with the loss of striatal

dopamine, and some patients with PD tremor do not improve or even

worsen with levodopa,35 it is generally believed that rest tremors are

modulated predominantly centrally by multiple generators within the

corticobasal ganglia and corticocerebellar circuitry. Functional neuro-

surgical treatments that inhibit pathways through the basal ganglia are

thought to work by disrupting these circuits.36

As ET becomes more severe it may occur at rest;37 however, this

can also sometimes represent coexistent PD or incomplete postural

relaxation.38 ET resting tremor is asymmetric and the frequency

Table 1. Classification of Tremor Etiology Based on Circumstances of Occurrence

Etiology Rest Tremor Action Tremor Notable Characteristics

Postural Kinetic

Parkinsonism +++ + + 3–6 Hz, can re-emerge with posture (re-emergent

tremor)

Midbrain (Holmes)

tremor

++ + + Irregular and large amplitude, variable delayed onset,

proximal as well as distal muscles involved

Thalamic tremor ++ ++ ++ Rare, sometimes delayed onset, can be associated with

pain or sensory symptoms

Essential tremor + +++ +++ 4–12 Hz, can occur at rest in longstanding disease, can

have intentional component and be associated with mild

ataxia or eye movement abnormalities

Cerebellar tremor + ++ ,5 Hz, predominantly intention tremor, uni- or

bilateral, often associated with other cerebellar

abnormalities such as dysmetria, overshoot, and past-

pointing

Exaggerated physiologic

tremor

++ ++ Non-pathological; generally between 6 and 12 Hz, can

result from anxiety or stress, fatigue, hypothermia,

hypoglycemia, or metabolic disorders such as

hyperthyroidism

Drug-induced tremor ++ ++ Non-progressive, usually symmetric, often has a dose-

response relationship with the causative drug and/or is

temporally related with drug onset

Orthostatic tremor +++ .13 Hz, occurs with weight bearing or isometric

muscle contraction, variable latent period

Dystonic tremor + ++ ++ Usually ,7 Hz or jerky and rhythmic irregular with

variable amplitude, accompanied by abnormal (some-

times subtle) posturing, often having a null point and/or

‘‘sensory trick’’

Neuropathic tremor + + ++ 3–6 Hz, predominantly affecting more distal muscles,

often irregular with variable amplitude, usually accom-

panied by symptoms of neuropathy

Task-specific

(e.g., writing tremor)

+ +++ 4–8 Hz, occurring predominantly with a specific task or

posture, most common form is primary writing tremor

+, sometimes noted; ++, usually noted; +++, characteristic.

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relationship between sides is variable.39 Though less commonly seen in

clinical practice, other diseases can produce rest tremors as well,

though usually not in isolation. Midbrain (rubral or Holmes) tremor

and thalamic tremor are occasional causes of rest tremor. Midbrain

tremor is caused by lesions of the cerebellothalamic and nigrostriatal

pathways and thus consists of a combination of rest, postural, and

kinetic components. The tremor at rest is of large amplitude and

irregular, and commonly involves both proximal and distal muscles at

frequencies of 2–5 Hz.4,40 Infarction in the midbrain is the most

common cause, though tumor, abscess and demyelination are

occasionally reported. Thalamic tremor is relatively rare, and causes

action and sometimes rest tremor due to lesions most often affecting

the ventral lateral posterior nucleus of the thalamus.41 Though DT

and drug-induced tremors are more commonly thought of as action

tremors, they can occur at rest, usually along with an action

component.

Action tremors

Most pathologic tremors are predominantly action tremors, whether

kinetic or postural (or often a combination of both). Unlike rest tremor,

the diagnostic possibilities of action tremor are broader, and discussion

based on etiology is more appropriate.

Action tremor in PD

Patients with PD can exhibit a variable-onset delayed tremor when

holding up an outstretched arm, with a frequency typical of PD rest

tremor. This is in contrast with the postural tremor of ET, which has

no delay in onset. It is commonly thought of as re-emergent PD rest

tremor, though a case of such tremor without rest tremor has been

reported.42 In addition, higher frequency 5–8 Hz lower amplitude

action tremors are not uncommon in PD and can be difficult to

distinguish from ET.4 Single photon emission computed tomography

imaging of the dopamine transporter has been approved in the United

Figure 2. Electromyography (EMG) Profile, Movement Analysis, and Frequency Spectrum of Rest Tremor in a Patient with Parkinson Disease(PD). (A) EMG profile. The first four traces represent surface EMG signal from forearm muscles; ECR, extensor carpi radialis; FCR, flexor carpi radialis. The bottom two

traces reflect displacement (darker line) derived from accelerometry. Note the relatively sinusoidal tremor displacement in the symptomatic left hand. (B) Frequency spectrum

of tremor displacement demonstrating a peak between 4 and 6 Hz in the symptomatic left (gray line) hand, with a trace peak present in the right (black line) hand.

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States of America to help differentiate these entities, and computerized

tremor analysis can also be useful in this regard.

Essential tremor

ET is the most prevalent adult movement disorder. It is often

familial and transmitted in an autosomal dominant pattern with high

penetrance.43 While advancing age is the most obvious risk factor, ET

can occur in the pediatric age group as well.44 Figure 3 shows a typical

EMG profile and frequency spectrum.

ET is generally a slowly progressive, clinically monosymptomatic

disorder marked by initially low-amplitude tremors (which can

increase dramatically as the disease progresses) of mid to high

frequency (4–12 Hz that decreases with age) and is most prominent in

the hands, though other body parts can be involved.4 The amplitude of

Figure 3. Electromyography (EMG) Profile, Movement Analysis, and Frequency Spectrum of Postural Tremor in a Patient with EssentialTremor (ET) with Arms Extended. (A) EMG profile. The first four traces represent surface EMG signal from forearm muscles; ECR, extensor carpi radialis; FCR,

flexor carpi radialis. The bottom two traces reflect displacement (darker line) derived from accelerometry (B) Frequency spectrum of tremor displacement demonstrating

a broad peak between 4 and 8 Hz in both hands.

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kinetic tremor (which is invariably present) is generally greater than

that of postural tremor.45 A worsening of kinetic tremor as the hand

approaches a target (intention tremor) can be seen.30 Head tremor

(commonly in the horizontal plane) can develop or rarely be present in

isolation, and a jaw tremor (in contrast to the lower lip tremor typically

associated with PD) can be seen in some cases.30 Unlike tremor in PD,

it is more irregular and more bilaterally symmetric, and it does not

occur as a hemibody tremor lateralized to one arm and leg.

Cogwheeling is often found secondary to tremor and should not be

confused with the rigidity seen in PD patients. The amelioration of

tremor with alcohol is common and can help establish the diagnosis,

and moderate use of alcohol limited to occasional social settings is

usually not discouraged. However, alcohol clearly should not be used

in the chronic treatment of ET, and the risk of dependence and abuse

in ET has not been completely addressed by formal studies.46

Cerebellar tremor

Cerebellar postural and action tremors are irregular and often of

high amplitude, causing severe functional disability. With no rest

component, patients may appear normal until they initiate movement

or assume a steady posture, and tremor is most pronounced with

intention.47 Irregular postural tremor of the head and rhythmic

postural sway (truncal tremor) may also occur. As with all tremors, the

frequency of cerebellar tremor depends upon the part of the body that

is affected.4 Tremor frequencies range from 3–8 Hz in the upper

extremities, around 1–3 Hz in the lower extremities, and 2–4 Hz in the

trunk. Injury to the deep cerebellar nuclei and cerebellar outflow tracts

are likely involved in tremor production. The benefits of both

pharmacologic and surgical treatments have been limited.4,48

Orthostatic tremor

The term orthostatic tremor (OT) was first used in 198449 and was

previously referred to as ‘‘shaky leg syndrome’’. In this relatively

uncommon but distinct disorder, patients find it increasingly difficult to

stand still due to sensations variably described as tremor, unsteadiness,

and/or pain. Tasks such as waiting in line or doing dishes become

troublesome, and patients find themselves needing to walk in place,

continuously shift their weight from one leg to the other, or lean

against a wall in order to reduce discomfort.50 OT may also be

associated with muscle cramps,51 and patients will often describe

subjective tremor elsewhere in the body, such as the lips, jaws, or

hands. Significant disability and depression with substantial curtailing

of activities can occur in severe cases.

OT is more common in women, with a mean age of onset in the

early sixties, and is generally considered to be sporadic, though

associations with various other neurologic disorders have been

reported, including ET, PD, cerebellar degeneration, progressive

supranuclear palsy, and pontine lesions.52–54 Familial occurrence is

uncommon, though EMG-confirmed OT in three brothers has been

reported.53,55

The diagnosis of OT should be suspected in any patient

describing pain or other unpleasant sensations shortly after

standing that is relieved by sitting or walking. Auscultation of

the gastrocnemius muscles can sometimes reveal a characteristic of

barely audible noise akin to the sound of a helicopter.56 The

diagnosis is confirmed by pathognomonic surface EMG recordings

revealing rhythmic activation of lower limb muscles at sharply

peaked frequencies between 14 and 18 Hz, and sometimes higher

(Figure 4).

Frequency spectra consistently show a high degree of coherence

between limbs, unlike that in any other form of tremor.

The etiology of OT is unclear; while it was initially considered

a task-specific tremor, upright body position has been shown to be

less important than weight-bearing and the sensation of postural

instability, both of which may give rise to the clinical disorder. It

has been demonstrated in all limbs in OT patients with weight

bearing57 and isometric contraction,58 and high-frequency highly

coherent tremor has been produced in normal subjects made to

feel unsteady through postural manipulation or galvanic stimula-

tion, suggesting an exaggerated response to postural instability as

playing a role.59 These observations, combined with its demon-

stration in cranially innervated muscles60 and the resetting of

tremor phase induced with transcranial magnetic stimulation61

support a supraspinal central generator of the tremor. Treatment

of OT is often disappointing, and improvement has been reported

mostly with clonazepam, but occasionally with phenobarbital,

primidone, or valproate.62 Improvement with deep brain stimula-

tion (DBS) of the ventrointermediate nucleus (VIM) has also been

described.63,64

Dystonic tremor

DT occurs in a body part affected by dystonia. It is typically postural

or task related, with an irregular or jerky rhythmic low- to mid-

frequency tremor secondary to co-contraction of agonist and

antagonist muscles. Frequencies range from 1 to 6 Hz during dystonic

contractions, with higher frequencies similar to ET seen during

voluntary movements.4 Tremor associated with dystonia (occurring in

a clinically non-dystonic body part in a patient with dystonia) can also

occur.47 Characteristic of DT is the null point, a position in which the

tremor almost fully abates.65 It may initially be present during specific

action but can generalize to occur with any task. DT of the head or

hand can sometimes be confused with ET or PD, and patients with DT

have been postulated to account for some of the instances of patients

with parkinsonism who have normal dopamine neuroimaging (scans

without evidence of dopaminergic deficit (SWEDDs), or scans without

evidence of dopaminergic deficit).66 Careful evaluation for subtle

dystonic posturing and the presence of a null point and/or geste

antagoniste (a tactile or proprioceptive sensory trick that reduces the

abnormal posture), as well as attention to tremor quality (jerky versus

smooth), are helpful in making the correct diagnosis.47 In patients with

head tremor, it is also helpful to remember that the typical head

tremor seen in ET rarely occurs in the absence of coexistent hand

tremor.30

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Neuropathic tremor

Neuropathic tremor is thought to arise secondary to central processing

of mistimed and distorted peripheral input that occurs with neuropathic

disease.67 It is usually irregular and distal, and can be asymmetric or

relatively symmetric, with frequencies in the upper limbs ranging from 3

to 6 Hz. Figure 5 demonstrates the distal low frequency tremor that

developed subacutely in a patient with sensorimotor neuropathy with

demyelinating and axonal features. Neuropathic tremor can physiolo-

gically mimic a number of other tremor disorders, and the most helpful

clues to the diagnosis are the coexistence of neuropathic symptoms.4 It

can occur at rest, with posture, or during movement and can develop

with multiple neuropathies, such as anti-myelin-associated glycoprotein

Figure 4. Electromyography (EMG) Profile and Frequency Spectrum of A Patient with Orthostatic Tremor While Standing. (A) EMG profile. GM,

gastrocnemius; Hamst, hamstrings; TA, tibialis anterior; VL, vastus lateralis. (B) Frequency spectra demonstrating a sharp peak at 17.3 Hz in all muscles recorded. (C)

Note the high coherence between frequency spectra of the EMG signals in the legs.

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(anti-MAG) neuropathy.68 Most patients with neuropathic tremor are

without central nervous system disease, and the tremor subsides with

treatment of underlying neuropathy. Beta-blockers and other drugs used

in ET have been reported to be helpful for neuropathic tremor, and

success with VIM DBS has also been reported.69

Task-specific tremor

Tremor (not associated with abnormal postures or muscle spasm)

that occurs predominantly during the execution of a specific (and often

skilled) task is considered a task-specific tremor.43 While the 4–8 Hz

tremor of primary writing tremor (PWT) is the most common example

Figure 5. Electromyography (EMG) Profile, Movement Analysis, and Frequency Spectrum of a Patient with Neuropathic Tremor Accompaniedby Bilateral Sensory Loss and Weakness. EMG and nerve conduction studies demonstrated sensorimotor neuropathy with both demyelinating and axonal

features. Note the distal low-frequency tremor driven primarily by wrist flexors and extensors with little proximal limb involvement. (A) EMG profile. The first six traces

represent surface EMG signal from arm muscles. ECR, extensor carpi radialis; FCR, flexor carpi radialis; Tric, triceps. The bottom two traces reflect displacement

(darker line) derived from accelerometry. (B) Frequency spectrum of tremor displacement demonstrating peaks between 4 and 6 Hz.

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of a task-specific tremor, it can be found in musicians, athletes, and

other professionals who are highly trained, such as surgeons or dentists.

PWT can be sporadic or inherited in an autosomal dominant manner,

and its etiology is controversial; it has been proposed to be a variant of

DT, ET, and its own distinct entity.70 Poly-EMG profiles most

commonly show alternating contraction of agonist and antagonist

muscles, although various other contraction patterns can be seen as

well. Figure 6 shows co-contraction of agonist and antagonist muscles

and excessive muscle activity resulting in 4–5 Hz irregular tremor in a

patient with primary writing tremor of 10 years’ duration.4

Drug-induced tremor

A wide variety of pharmacologic agents with differing mechanisms

of action can cause tremor as a side effect.4 In general, they are

Figure 6. Electromyography (EMG) Profile, Movement Analysis, and Frequency Spectrum of a Patient with Primary Writing Tremor whileWriting with the Dominant Hand. Co-contraction of agonist and antagonist muscles below the deltoid is evident, though alternating contraction of agonist and

antagonist muscles may be a more commonly seen pattern. (A) EMG profile. The first five traces represent surface EMG signal from forearm muscles. ECR, extensor

carpi radialis; FCR, flexor carpi radialis. The bottom two traces reflect displacement (darker line) derived from accelerometry (B) Frequency spectrum of tremor

displacement demonstrating peaks between 4 and 6 Hz.

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non-progressive, often temporally related to the onset of a medication,

and worsen with increasing medication dose.71 Drug-induced rest

tremor can occur in isolation or as part of drug-induced parkinsonism

secondary to the use of antipsychotics, and can be clinically

indistinguishable from PD tremor.72 In addition to neuroleptics, any

medication which can cause secondary parkinsonism, such as lithium

carbonate, valproate, or serotonin specific reuptake inhibitors, can

induce a rest tremor.73,74

Many of these medications can cause an action tremor as well.

Lithium is a frequent offender, causing tremor at both toxic and

therapeutic levels.75,76 High blood levels of lithium are not necessary to

produce tremor,77,78 and no correlation has been found between blood

lithium levels and patient complaints of tremor.79 Non-toxic lithium

tremor can occur acutely within the first week of starting therapy,80 or

may develop within weeks81 or months after starting the medication.78

Valproate can cause a fine, 6–9 Hz rhythmic postural tremor, similar

to the action tremor, which can occur with tricyclic antidepressants,

and can mimic ET.71 Treatment with propranolol can be beneficial.82

Other tremorogenic medications include anti-arrhythmics, broncho-

dilators, and chemotherapeutic agents.83,84 Drugs of abuse such as

alcohol, cocaine, and amphetamines can also cause tremor, due to

acute intoxication, chronic use, or withdrawal.85 Similar effects can be

seen with heavy caffeine use.

Psychogenic tremor

Psychogenic tremors can occur as a manifestation of an underlying

psychiatric disorder such as somatoform or factitious disorder, or can

occur in cases of malingering.86 The diagnosis is based on unusual

phenomenology and other diagnostic clues, such as abrupt onset,

inconsistencies in tremor pattern and characteristics, spontaneous

remissions, response to placebo, and distractibility.47,87,88 Relatively

consistent physiologic findings include an increase in tremor amplitude

with inertial loading (Figure 7), large fluctuations in frequency and

amplitude, co-activation of antagonist muscles at the onset of tremor,

and the absence of finger tremors.89–91 Coexistent non-physiologic

signs such as weakness or sensory abnormalities and underlying

psychopathology can also help to suggest the diagnosis. Because it may

be difficult to approach patients with a diagnosis of psychogenic

tremor, clinicians are often reluctant to discuss the possibility of

psychogenicity. However, if correctly identified, psychogenic tremor

due to a somatoform disorder is potentially curable through a

coordinated effort between neurologists and psychiatrists.92 It is

important to remember that the diagnosis of psychogenic tremor can

only be made by a neurologist, while the role of the psychiatrist is to

explore underlying psychodynamics and the degree of insight, guide

psychopharmacologic treatments, and provide the continued psy-

chotherapy critical for improvement.73

Other types of tremor

Some disorders, such as asterixis, epilepsia partialis continua, and

rhythmic forms of myoclonus such as palatal myoclonus, are often

misinterpreted as tremor. Physiologically, myoclonic EMG bursts do

not have gradual rise times and are not sinusoidal, and are separated

by discrete periods of muscle silence.3 Cortical tremor is thought to be

Figure 7. Electromyography (EMG) Profile and Movement Analysis of a Patient with Psychogenic Tremor of the Left Arm with the ArmExtended (left) and with Inertial Loading of the Extended Left Hand (right). Note the almost fivefold increase in tremor amplitude as shown by an increase in

mean displacement from 0.9 to 4.9 mm.

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a variant of action-induced myoclonus in the setting of cortical

myoclonus.93 It is characterized by distal short duration (generally less

than 50 ms) rhythmic irregular bursts on EMG with synchronous

activation of agonist and antagonist muscles and alternating periods of

near silence. Peak EMG burst frequency is 9–18 Hz with an associated

cortical potential on EEG back-averaging.91,94

Summary

While clinical assessment remains the most commonly used method

of diagnosing and examining tremor, the techniques of computerized

quantitative analysis using accelerometry, EMG, and spiral analysis

can be powerful tools in the assessment of tremor in both clinical and

research paradigms. A combination of careful clinical evaluation,

response to therapy, and computerized analysis best helps distinguish

the various pathologic tremors and shed light on their pathogenesis.

References

1. Marsden CD. Origins of normal and pathological tremor. In: Findley LJ,

Capildeo R, eds. Movement Disorders: Tremor. New York: Oxford University Press;

1988:37–84.

2. Findley LJ. Classification of tremors. J Clin Neurophysiol 1996;13:122–132,

http://dx.doi.org/10.1097/00004691-199603000-00003.

3. Deuschl G, Raethjen J, Lindemann M, Krack P. The pathophysiology of

tremor. Muscle Nerve 2001;24:716–35, http://dx.doi.org/10.1002/mus.1063.

4. Elble RJ, Koller WC. Tremor. Baltimore: The Johns Hopkins University

Press; 1990.

5. Louis ED, Barnes L, Wendt KJ, et al. A teaching videotape for the

assessment of essential tremor. Mov Disord 2001;16:89–93, http://dx.doi.org/

10.1002/1531-8257(200101)16:1,89::AID-MDS1001.3.0.CO;2-L.

6. Fahn S, Tolosa E, Concepcion M. Clinical rating scale for tremor. In:

Jankovic J, Tolosa E, eds. Parkinson’s Disease and Movement Disorders, 2nd ed.

Baltimore: Williams and Wilkins; 1993:271–80.

7. Bain PG, Findley LJ. Assessing Tremor Severity. London: Smith-Gordon and

Compant, Ltd; 1993.

8. Elble RJ, Comella C, Fahn S, et al. The essential tremor rating assessment

scale (TETRAS). Mov Disord 2008;23:S357.

9. Louis ED, Ford B, Bismuth B. Reliability between two observers using a

protocol for diagnosing essential tremor. Mov Disord 1998;13:287–293, http://

dx.doi.org/10.1002/mds.870130215.

10. Stacy MA, Elble RJ, Ondo WG, Wu SC, Hulihan J. Assessment of

interrater and intrarater reliability of the Fahn-Tolosa-Marin Tremor Rating

Scale in essential tremor. Mov Disord 2007;22:833–838, http://dx.doi.org/10.

1002/mds.21412.

11. Pullman SL. Spiral analysis: a new technique for measuring tremor with

a digitizing tablet. Mov Disord 1998;13:85–89, http://dx.doi.org/10.1002/mds.

870131315.

12. Glaser EM, Ruchkin DS. Principles of Neurobiological Signal Analysis. New

York: Academic Press; 1976.

13. Findley LJ, Koller WC. Essential tremor: a review. Neurology 1984;37:

1194–1197, http://dx.doi.org/10.1212/WNL.37.7.1194.

14. Marsden CD. Origins of normal and pathological tremor. In: Findley LJ,

Capildeo R, eds. Movement Disorders: Tremor. New York: Oxford University Press;

1984:37–84.

15. Pullman SL, Fahn S, Rueda J. Physiologic characterization of dystonic

and essential tremors. Neurology 1992;42:471, http://dx.doi.org/10.1212/WNL.

42.3.471.

16. Pullman SL, Goodin DS, Marquinez AI, Tabbal S, Rubin M. Clinical

utility of surface EMG: report of the therapeutics and technology assessment

subcommittee of the American Academy of Neurology. Neurology 2000;55:171–

177, http://dx.doi.org/10.1212/WNL.55.2.171.

17. Elble RJ. Physiologic and essential tremor. Neurology 1986;36:225–231,

http://dx.doi.org/10.1212/WNL.36.2.225.

18. Louis ED, Ford B, Pullman S, Baron K. How normal is ‘normal’? Mild

tremor in a multiethnic cohort of normal subjects. Arch Neurol 1998;55:222–227,

http://dx.doi.org/10.1001/archneur.55.2.222.

19. Critchley E. Clinical manifestations of essential tremor. J Neurol Neurosurg

Psychiatry 1972;35:365–372, http://dx.doi.org/10.1136/jnnp.35.3.365.

20. Hubble JP, Busenbark KL, Koller WC. Essential tremor. Clin

Neuropharmacol 1989;12:453–482, http://dx.doi.org/10.1097/00002826-

198912000-00001.

21. Elble RJ, Pullman SL, Matsumoto JY, Raethjen J, Deuschl G,

Tintner R. Tremor amplitude is logarithmically related to 4- and 5-point

tremor rating scales. Brain 2006;129:2660–2666, http://dx.doi.org/10.1093/

brain/awl190.

22. Elble RJ, Brilliant M, Leffler K, Higgins C. Quantification of essential

tremor in writing and drawing. Mov Disord 1996;11:70–78, http://dx.doi.org/

10.1002/mds.870110113.

23. Gescheider GA. Psychophysics: The Fundamentals. 3rd ed. Mahwah, NJ: L.

Erlbaum Associates; 1997.

24. Stanley K, Hagenah J, Bruggemann N, et al. Digitized spiral analysis

is a promising early motor marker for Parkinson Disease. Parkinsonism Relat

Disord 2010;16:233–234, http://dx.doi.org/10.1016/j.parkreldis.2009.12.007.

25. Hallett M. Overview of human tremor physiology. Mov Disord 1998;13:

43–48, http://dx.doi.org/10.1002/mds.870131308.

26. Mure H, Hirano S, Tang CC, et al. Parkinson’s disease tremor-related

metabolic network: characterization, progression, and treatment effects.

Neuroimage 2011;54:1244–1253, http://dx.doi.org/10.1016/j.neuroimage.

2010.09.028.

27. Timmermann L, Gross J, Dirks M, Volkmann J, Freund HJ, Schnitzler

A. The cerebral oscillatory network of parkinsonian resting tremor. Brain 2003;

126:199–212, http://dx.doi.org/10.1093/brain/awg022.

28. Louis ED, Okun MS. It is time to remove the ‘benign’ from the essential

tremor label. Parkinsonism Relat Disord 2011;17:516–520, http://dx.doi.org/10.

1016/j.parkreldis.2011.03.012.

29. Louis ED. Essential tremor: evolving clinicopathological concepts in an

era of intensive post-mortem enquiry. Lancet Neurol 2010;9:613–622, http://dx.

doi.org/10.1016/S1474-4422(10)70090-9.

30. Louis ED. Essential tremor. Handb Clin Neurol 2011;100:433–448, http://

dx.doi.org/10.1016/B978-0-444-52014-2.00033-1.

31. Deuschl G, Elble RJ. The pathophysiology of essential tremor. Neurology

2000;54:S14–20, http://dx.doi.org/10.1212/WNL.54.4.14A.

Tremor Phenomenology and Assessment Hess CW, Pullman SL

Tremor and Other Hyperkinetic Movementshttp://www.tremorjournal.org

The Center for Digital Research and ScholarshipColumbia University Libraries/Information Services13

32. Moore GP, Ding L, Bronte-Stewart HM. Concurrent Parkinson tremors.

J Physiol 2000;529:273–281, http://dx.doi.org/10.1111/j.1469-7793.2000.

00273.x.

33. Lauk M, Koster B, Timmer J, Guschlbauer B, Deuschl G, Lucking CH.

Side-to-side correlation of muscle activity in physiological and pathological

human tremors. Clin Neurophysiol 1999;110:1774–1783, http://dx.doi.org/10.

1016/S1388-2457(99)00130-3.

34. Raethjen J, Lindemann M, Schmaljohann H, Wenzelburger R, Pfister

G, Deuschl G. Multiple oscillators are causing parkinsonian and essential

tremor. Mov Disord 2000;15:84–94, http://dx.doi.org/10.1002/1531-

8257(200001)15:1,84::AID-MDS1014.3.0.CO;2-K.

35. Hallett M, Deuschl G. Are we making progress in the understanding of

tremor in Parkinson’s disease? Ann Neurol 2010;68:780–781, http://dx.doi.org/

10.1002/ana.22253.

36. Deuschl G, Raethjen J, Baron R, Lindemann M, Wilms H, Krack P.

The pathophysiology of parkinsonian tremor: a review. J Neurol 2000;247 Suppl

5:V33–48, http://dx.doi.org/10.1007/PL00007781.

37. Louis ED, Asabere N, Agnew A, et al. Rest tremor in advanced essential

tremor: a post-mortem study of nine cases. J Neurol Neurosurg Psychiatry 2011;82:

261–265, http://dx.doi.org/10.1136/jnnp.2010.215681.

38. Elble RJ, Deuschl G. An update on essential tremor. Curr Neurol Neurosci

Rep 2009;9:273–277, http://dx.doi.org/10.1007/s11910-009-0041-6.

39. Cohen O, Pullman S, Jurewicz E, Watner D, Louis ED. Rest tremor in

patients with essential tremor: prevalence, clinical correlates, and electro-

physiologic characteristics. Arch Neurol 2003;60:405–410, http://dx.doi.org/10.

1001/archneur.60.3.405.

40. Paviour DC, Jager HR, Wilkinson L, Jahanshahi M, Lees AJ. Holmes

tremor: application of modern neuroimaging techniques. Mov Disord 2006;21:

2260–2262, http://dx.doi.org/10.1002/mds.20981.

41. Krystkowiak P, Martinat P, Cassim F, et al. Thalamic tremor:

correlations with three-dimensional magnetic resonance imaging data and

pathophysiological mechanisms. Mov Disord 2000;15:911–918, http://dx.doi.

org/10.1002/1531-8257(200009)15:5,911::AID-MDS1023.3.0.CO;2-B.

42. Louis ED, Pullman SL, Eidelberg D, Dhawan V. Re-emergent tremor

without accompanying rest tremor in Parkinson’s disease. Can J Neurol Sci 2008;

35:513–515.

43. Deuschl G, Bain P, Brin M. Consensus statement of the Movement

Disorder Society on Tremor. Ad Hoc Scientific Committee. Mov Disord 1998;

13:2–23, http://dx.doi.org/10.1002/mds.870131303.

44. Louis ED, Dure LS, Pullman S. Essential tremor in childhood: a series

of nineteen cases. Mov Disord 2001;16:921–923, http://dx.doi.org/10.1002/

mds.1182.

45. Brennan KC, Jurewicz EC, Ford B, Pullman SL, Louis ED. Is essential

tremor predominantly a kinetic or a postural tremor? A clinical and

electrophysiological study. Mov Disord 2002;17:313–316, http://dx.doi.org/10.

1002/mds.10003.

46. Hess CW, Saunders-Pullman R. Movement disorders and alcohol

misuse. Addict Biol 2006;11:117–125, http://dx.doi.org/10.1111/j.1369-1600.

2006.00017.x.

47. Deuschl G, Bain P, Brin M. Consensus statement of the Movement

Disorder Society on Tremor. Ad Hoc Scientific Committee. Mov Disord 1998;13

Suppl 3:2–23.

48. Jankovic J, Cardoso F, Grossman RG, Hamilton WJ. Outcome after

stereotactic thalamotomy for parkinsonian, essential, and other types of tremor.

Neurosurgery 1995;37:680–686; discussion 6–7, http://dx.doi.org/10.1227/

00006123-199510000-00011.

49. Heilman KM. Orthostatic tremor. Arch Neurol 1984;41:880–881, http://

dx.doi.org/10.1001/archneur.1984.04050190086020.

50. Gerschlager W, Brown P. Orthostatic tremor—a review. Handb Clin

Neurol 2011;100:457–462, http://dx.doi.org/10.1016/B978-0-444-52014-2.

00035-5.

51. FitzGerald PM, Jankovic J. Orthostatic tremor: an association with

essential tremor. Mov Disord 1991;6:60–64, http://dx.doi.org/10.1002/mds.

870060111.

52. de Bie RM, Chen R, Lang AE. Orthostatic tremor in progressive

supranuclear palsy. Mov Disord 2007;22:1192–1194, http://dx.doi.org/10.

1002/mds.21434.

53. Gerschlager W, Munchau A, Katzenschlager R, et al. Natural history

and syndromic associations of orthostatic tremor: a review of 41 patients. Mov

Disord 2004;19:788–795, http://dx.doi.org/10.1002/mds.20132.

54. Piboolnurak P, Yu QP, Pullman SL. Clinical and neurophysiologic

spectrum of orthostatic tremor: case series of 26 subjects. Mov Disord 2005;20:

1455–1461, http://dx.doi.org/10.1002/mds.20588.

55. Fischer M, Kress W, Reiners K, Rieckmann P. Orthostatic tremor in

three brothers. J Neurol 2007;254:1759–1760, http://dx.doi.org/10.1007/

s00415-007-0647-z.

56. Brown P. New clinical sign for orthostatic tremor. Lancet 1995;346:306–

307, http://dx.doi.org/10.1016/S0140-6736(95)92190-7.

57. Boroojerdi B, Ferbert A, Foltys H, Kosinski CM, Noth J, Schwarz M.

Evidence for a non-orthostatic origin of orthostatic tremor. J Neurol Neurosurg

Psychiatry 1999;66:284–288, http://dx.doi.org/10.1136/jnnp.66.3.284.

58. Walker FO, McCormick GM, Hunt VP. Isometric features of orthostatic

tremor: an electromyographic analysis. Muscle Nerve 1990;13:918–922, http://

dx.doi.org/10.1002/mus.880131006.

59. Sharott A, Marsden J, Brown P. Primary orthostatic tremor is an

exaggeration of a physiological response to instability. Mov Disord 2003;18:195–

199, http://dx.doi.org/10.1002/mds.10324.

60. Koster B, Lauk M, Timmer J, et al. Involvement of cranial muscles and

high intermuscular coherence in orthostatic tremor. Ann Neurol 1999;45:384–

388, http://dx.doi.org/10.1002/1531-8249(199903)45:3,384::AID-ANA15.

3.0.CO;2-J.

61. Manto MU, Setta F, Legros B, Jacquy J, Godaux E. Resetting of

orthostatic tremor associated with cerebellar cortical atrophy by transcranial

magnetic stimulation. Arch Neurol 1999;56:1497–500, http://dx.doi.org/10.

1001/archneur.56.12.1497.

62. Wasielewski PG, Burns JM, Koller WC. Pharmacologic treatment of

tremor. Mov Disord 1998;13:90–100, http://dx.doi.org/10.1002/mds.

870131316.

63. Guridi J, Rodriguez-Oroz MC, Arbizu J, et al. Successful thalamic deep

brain stimulation for orthostatic tremor. Mov Disord 2008;23:1808–1811, http://

dx.doi.org/10.1002/mds.22001.

64. Magarinos-Ascone C, Ruiz FM, Millan AS, et al. Electrophysiological

evaluation of thalamic DBS for orthostatic tremor. Mov Disord 2010;25:2476–

2477, http://dx.doi.org/10.1002/mds.23333.

Hess CW, Pullman SL Tremor Phenomenology and Assessment

Tremor and Other Hyperkinetic Movementshttp://www.tremorjournal.org

The Center for Digital Research and ScholarshipColumbia University Libraries/Information Services14

65. Gironell A, Kulisevsky J. Diagnosis and management of essential tremor

and dystonic tremor. Ther Adv Neurol Disord 2009;2:215–222, http://dx.doi.org/

10.1177/1756285609104791.

66. Bain PG. Dystonic tremor presenting as parkinsonism: long-term follow-

up of SWEDDs. Neurology 2009;72:1443–1445, http://dx.doi.org/10.1212/

WNL.0b013e3181a18809.

67. Deuschl G, Bergman H. Pathophysiology of nonparkinsonian tremors.

Mov Disord 2002;17 Suppl 3:S41–48, http://dx.doi.org/10.1002/mds.10141.

68. Pedersen SF, Pullman SL, Latov N, Brannagan TH, 3rd. Physiological

tremor analysis of patients with anti-myelin-associated glycoprotein associated

neuropathy and tremor. Muscle Nerve 1997;20:38–44, http://dx.doi.org/10.

1002/(SICI)1097-4598(199701)20:1,38::AID-MUS5.3.0.CO;2-I.

69. Weiss D, Govindan RB, Rilk A, et al. Central oscillators in a patient with

neuropathic tremor: evidence from intraoperative local field potential recordings.

Mov Disord 2011;26:323–327, http://dx.doi.org/10.1002/mds.23374.

70. Bain PG. Task-specific tremor. Handb Clin Neurol 2011;100:711–718,

http://dx.doi.org/10.1016/B978-0-444-52014-2.00050-1.

71. Morgan JCS, K.D. Drug-induced tremors. Lancet Neurol 2005;4:866–876,

http://dx.doi.org/10.1016/S1474-4422(05)70250-7.

72. Lorberboym M, Treves TA, Melamed E, Lampl Y, Hellmann M,

Djaldetti R. [123I]-FP/CIT SPECT imaging for distinguishing drug-induced

parkinsonism from Parkinson’s disease. Mov Disord 2006;21:510–514, http://dx.

doi.org/10.1002/mds.20748.

73. Fahn S, Jankovic J. Principles and Practice of Movement Disorders.

Philadelphia: Churchill Livingstone/Elsevier; 2007.

74. Zadikoff C, Munhoz RP, Asante AN, et al. Movement disorders in

patients taking anticonvulsants. J Neurol Neurosurg Psychiatry 2007;78:147–151,

http://dx.doi.org/10.1136/jnnp.2006.100222.

75. Bunney WE, Wehr TR, Gillin JC, Post RM, Goodwin FK, van

Kammen DP. The switch process in manic-depressive psychosis. Ann Intern Med

1977;87:319–335.

76. Prien RF. Lithium in the treatment of affective disorders. Clin

Neuropharmacol 1978;3:113–131, http://dx.doi.org/10.1097/00002826-

197800030-00008.

77. Lapierre YD. Control of lithium tremor with propranolol. Can Med Assoc

J 1976;114:619–620.

78. Tyrer P, Shopsin B. Neural and neuromuscular side effects of lithium. In:

Johnson FN, ed. Handbook of Lithium Therapy. Lancaster: MTP Press; 1980:289–309.

79. Vestergaard P, Poulstrup I, Schou M. Prospective studies on a lithium

cohort. 3. Tremor, weight gain, diarrhea, psychological complaints. Acta

Psychiatry Scand 1988:434–441, http://dx.doi.org/10.1111/j.1600-0447.1988.

tb06363.x.

80. Pullinger S, Tyrer P. Acute lithium-induced tremor. Br J Psychiatry 1983;

143:40–41, http://dx.doi.org/10.1192/bjp.143.1.40.

81. Brown WT. The pattern of lithium side effects and toxic reactions in the

course of lithium therapy. In: Handbook of Lithium Therapy. Baltimore: University

Park Press; 1980:Chapter 33.

82. Karas BJ, Wilder BJ, Hammond EF, Bauman AW. Treatment of

valproate tremors. Neurology 1983;33:1380–1382, http://dx.doi.org/10.1212/

WNL.33.10.1380.

83. Coulter DM, Edwards IR, Savage RL. Survey of neurological problems

with amiodarone in the New Zealand Intensive Medicines Monitoring

Programme. N Z Med J 1990;103:98–100.

84. Puschmann A, Wszolek ZK. Diagnosis and treatment of common forms

of tremor. Semin Neurol 2011;31:65–77, http://dx.doi.org/10.1055/s-0031-

1271312.

85. Hess C, Saunders-Pullman R. Hyperkinetic movement disorders. In:

Verster JC, Conrod P, Brady K, Galanter M, eds. Drug Abuse and Addiction in

Medical Illness. New York: Springer; July 2012.

86. Marjama J, Troster AI, Koller WC. Psychogenic movement disorders.

Neurol Clin 1995;13:283–297.

87. Kim YJ, Pakiam AS, Lang AE. Historical and clinical features of

psychogenic tremor: a review of 70 cases. Can J Neurol Sci 1999;26:190–195.

88. Koller W, Lang A, Vetere-Overfield B, et al. Psychogenic tremors.

Neurology 1989;39:1094–1099, http://dx.doi.org/10.1212/WNL.39.8.1094.

89. McAuley JH, Rothwell JC, Marsden CD, Findley LJ. Electro-

physiological aids in distinguishing organic from psychogenic tremor. Neurology

1998;50:1882–1884, http://dx.doi.org/10.1212/WNL.50.6.1882.

90. Piboolnurak P, Rothey N, Ahmed A, et al. Psychogenic tremor disorders

identified using tree-based statistical algorithms and quantitative tremor

analysis. Mov Disord 2005;20:1543–1549, http://dx.doi.org/10.1002/mds.

20634.

91. Zeuner KE, Shoge RO, Goldstein SR, Dambrosia JM, Hallett M.

Accelerometry to distinguish psychogenic from essential or parkinsonian

tremor. Neurology 2003;61:548–550, http://dx.doi.org/10.1212/01.WNL.

0000076183.34915.CD.

92. Williams DT, Ford B, Fahn S. Phenomenology and psychopathology

related to psychogenic movement disorders. Adv Neurol 1995;65:231–257.

93. Regragui W, Gerdelat-Mas A, Simonetta-Moreau M. Cortical tremor

(FCMTE: familial cortical myoclonic tremor with epilepsy). Neurophysiol Clin

2006;36:345–349, http://dx.doi.org/10.1016/j.neucli.2006.12.005.

94. Toro C, Pascual-Leone A, Deuschl G, Tate E, Pranzatelli MR,

Hallett M. Cortical tremor. A common manifestation of cortical myoclonus.

Neurology 1993;43:2346–2353, http://dx.doi.org/10.1212/WNL.43.11.2346.

Tremor Phenomenology and Assessment Hess CW, Pullman SL

Tremor and Other Hyperkinetic Movementshttp://www.tremorjournal.org

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